The sites colonized by Neisseria gonorrhoeae within the human host are diverse and each site represents a unique niche with respect to nutrients, environmental factors and competing microorganisms. The growth environment has a marked effect on the metabolism and cellular composition of N. gonorrhoeae, and an altered cellular composition is often in the interaction of this microorganism with the human host (1). The overall goal of this project is to elucidate the specific mechanisms employed by N. gonorrhoeae for the assimilation of the essential nutrient iron. A majority of the parent project is focused on a study of the major iron binding protein in Neisseria commonly referred to as Fbp (ferric binding protein). While a great deal of biological and chemical data have been obtained on the Fbp, the precise role of this protein in the survival and pathogenesis of N. gonorrhoeae remains speculative (2,3). One attractive hypothesis is that Fbp functions in a central binding step that is essential for the assimilation of iron by the pathogenic Neisseria when grown under iron-restricted conditions. Expression of such a protein would thus be critical for the organism to obtain the iron necessary for growth. Clearly, the ability to obtain nutrients essential for growth is directly related to the ability of an organism to survive in vivo and ultimately to cause disease. The current project is based on the following specific aims: 1. To examine the regulation of Fbp expression by Fe. 2. To examine the possible influence of Fbp expression on gonococcal pathogenesis as assessed in a mouse chamber model (4). 3. To examine the molecular events involved in the transport of iron by identification of other proteins involved in iron transport and utilization. 4. To clone the genes involved in the transport of iron in N. gonorrhoeae.